Abstract

Atherosclerosis is a progressive disease of the large and medium-sized arteries. The disease is characterised by endothelial dysfunction, inflammation and the accumulation of fatty and fibrous substances in the vessel wall, resulting in thickening and loss of elasticity of the arteries. The word atherosclerosis has been derived from the Greek words "athera", porridge or gruel, and "skleros", hard or stiff. These words describe the external features of the lipid-loaded lesions that characterize the disease. Although atherosclerosis has been discovered in blood vessels of people living more than 3000 years ago, until the end of the 18th century its prevalence was very rare. During the 20th century, mortality caused by atherosclerosis strongly increased. Nowadays, complications of atherosclerosis are the main cause of death in the developed world, and are predicted to be the leading cause of death worldwide by the year 2020 (Fonarow, 2007). It is difficult to accurately determine the true frequency of atherosclerosis because it is a predominantly asymptomatic condition (Kavey et al., 2006). Early atherosclerotic lesions can already be found in the aorta shortly after birth, increasing in number during childhood. More advanced lesions begin to develop at an age of approximately 25 years. Generally, the clinical manifestations of the disease become apparent in the sixth decade of life. Symptomatic atherosclerotic disease most often involves the arteries supplying the heart, brain, kidneys, and lower extremities, and becomes apparent when arterial blood flow is obstructed. Complete occlusion of an affected artery can result in myocardial infarction, cerebral infarction, or peripheral vascular disease.

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F.G. Grosveld (Frank)
Erasmus University Rotterdam
Financial support by the Nederlandse Hartstichting for the printing of this thesis is gratefully acknowledged.
hdl.handle.net/1765/77017
Erasmus MC: University Medical Center Rotterdam

Samyn, H., & Moerland, M. (2009, March 18). Affected by abundant PLTP : the atherogenic role of a lipid transfer protein in transgenic mice. Retrieved from http://hdl.handle.net/1765/77017